帕金森病鼠旋转行为与谷胱甘肽表达

The rotation behaviour and glutathione expression in Parkinson's rats

目的 探讨延缓左旋多巴诱导运动障碍的可能机制。方法 采用左旋多巴治疗帕金森病鼠 ,观测左旋多巴诱导的旋转行为与脑纹状体区谷胱甘肽的改变。结果 左旋多巴诱导的旋转行为只在重度损伤的帕金森病鼠可见 ,于治疗 14d时达高峰为33r/min ,随治疗时间逐渐下降 ,治疗 2 2d为 2 3r/min ;左旋多巴治疗明显上调 ,重度和中度帕金森病鼠谷胱甘肽含量分别为 ( 8 82±0 89)mM/L和 ( 8 2 0± 0 35 )mM/L ,轻度损伤帕金森病鼠上调不明显。结论 左旋多巴诱导的旋转行为与帕金森病鼠多巴胺神经元缺失程度有关 ;谷胱甘肽上调不能阻止重度损伤帕金森病鼠中左旋多巴诱导的旋转行为 ,可能有益中度损伤帕金森病鼠。

Objective To investigate the possible mechanism of delaying dyskinesia induced by levodopa in parkinson's disease(PD).Methods The differently lesioned PD rats received twice daily levodopa or saline injection for three weeks.The behaviour and gluthatione(GSH) level were observed.Results The rotation behaviour induced by levodopa was observed only in severely lesioned PD rats,the peak point of rotation behaviour was 33 turns/min,the lower point of rotation behaviour was 23 turns/min after levodopa treatment for 22 days.Levodopa treatment obvioursly upregulated the level of striatum GSH in severely and moderately lesioned PD rats,each was (8.82±0.89)mM/L and (8.20±0.35)mM/L.Conclusion The rotation behaviour induced by levodopa was related with the differently lesioned degree PD rats,the upregulating level of striatum GSH in severely lesioned PD rats couldn't delay the rotation behaviour induced by levodopa treatement.GHS might be benefical in moderately lensioned PD rats.